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Micotherapy

Cytotoxic Constituents from the Sclerotia ofagainst Human Lung Adenocarcinoma Cells by Inducing Mitochondrial Apoptosis. 📎

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Abstract Title:

Cytotoxic Constituents from the Sclerotia ofagainst Human Lung Adenocarcinoma Cells by Inducing Mitochondrial Apoptosis.

Abstract Source:

Cells. 2018 Aug 24 ;7(9). Epub 2018 Aug 24. PMID: 30149516

Abstract Author(s):

Seulah Lee, Seul Lee, Hyun-Soo Roh, Seong-Soo Song, Rhim Ryoo, Changhyun Pang, Kwan-Hyuck Baek, Ki Hyun Kim

Article Affiliation:

Seulah Lee

Abstract:

Previous studies have revealed the antitumor potential ofWolf against a broad spectrum of cancers. However, the biological activity ofagainst lung cancer, which is known as the leading cause of cancer mortality worldwide, and its underlying chemical and molecular basis, remain to be investigated. We aimed to evaluate the in vitro cytotoxicity oftoward human lung adenocarcinoma cells with differentstatuses, to identify the bioactive constituents of, and explicate the molecular mechanisms underlying the cytotoxicity of these constituents in human lung adenocarcinoma cells. An EtOH extract of the sclerotia ofexhibited cytotoxicity toward four human lung cancer cell lines: A549, H1264, H1299, and Calu-6, regardless of theirstatus. Chemical investigation of the extract resulted in the isolation of two triterpenoids, dehydroeburicoic acid monoacetate () and acetyl eburicoic acid (); a sterol, 9,11-dehydroergosterol peroxide (); and a diterpenoid, dehydroabietic acid (). All of the isolated compounds were cytotoxic to the lung adenocarcinoma cell lines, exhibiting ICvalues ranging from 63.6μM to 171.0 μM at 48 h of treatment. The cytotoxicity of the extract and the isolated compounds were found to be mediated by apoptosis, and accompanied by elevated Bax expression and/or Bcl-2 phosphorylation along with caspase-3 activation. Our data demonstrate that the sclerotium ofand its four bioactive constituents (⁻) exert cytotoxicity against human lung adenocarcinoma cells, regardless of theirstatus, by inducing apoptosis associated with mitochondrial perturbation, and proposing the potential to employin the treatment of lung cancer.


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